Journal ArticleDOI
Mitochondria as sensors and regulators of calcium signalling
Reads0
Chats0
TLDR
During the past two decades calcium (Ca2+) accumulation in energized mitochondria has emerged as a biological process of utmost physiological relevance, opening new perspectives for investigation and molecular intervention.Abstract:
During the past two decades calcium (Ca(2+)) accumulation in energized mitochondria has emerged as a biological process of utmost physiological relevance. Mitochondrial Ca(2+) uptake was shown to control intracellular Ca(2+) signalling, cell metabolism, cell survival and other cell-type specific functions by buffering cytosolic Ca(2+) levels and regulating mitochondrial effectors. Recently, the identity of mitochondrial Ca(2+) transporters has been revealed, opening new perspectives for investigation and molecular intervention.read more
Citations
More filters
Journal ArticleDOI
Calcium and ROS: A mutual interplay.
TL;DR: Increasing evidence suggests a mutual interplay between calcium and ROS signaling systems which seems to have important implications for fine tuning cellular signaling networks.
Journal ArticleDOI
Endoplasmic reticulum-mitochondria contacts: function of the junction
Ashley A. Rowland,Gia K. Voeltz +1 more
TL;DR: The most well-characterized organelle contact sites are those between the endoplasmic reticulum (ER) and mitochondria, and the role of the ER–mitochondria junction in coordinating the functions of these two organelles is becoming clearer.
Journal ArticleDOI
Structure and function of ER membrane contact sites with other organelles.
TL;DR: The structure and functions of MCSs are described, primarily focusing on contacts of the ER with mitochondria and endosomes, as well as engaging in organelle biogenesis and dynamics.
Journal ArticleDOI
Mitochondria in the regulation of innate and adaptive immunity.
TL;DR: The evidence and mechanisms that mitochondrial dependent signaling controls innate and adaptive immune responses are discussed.
Journal ArticleDOI
13 reasons why the brain is susceptible to oxidative stress.
TL;DR: 13 reasons why the brain is susceptible to oxidative stress are rationalised and key reasons include inter alia unsaturated lipid enrichment, mitochondria, calcium, glutamate, modest antioxidant defence, redox active transition metals and neurotransmitter auto-oxidation.
References
More filters
Journal ArticleDOI
Calcium signalling: dynamics, homeostasis and remodelling
TL;DR: The Ca2+-signalling toolkit is used to assemble signalling systems with very different spatial and temporal dynamics and has a direct role in controlling the expression patterns of its signalling systems that are constantly being remodelled in both health and disease.
Journal ArticleDOI
Regulation of cell death: the calcium-apoptosis link.
TL;DR: The dual role of Ca2+ in living organisms is discussed in this paper, where it has been shown that cellular Ca 2+ overload, or perturbation of intracellular Ca2 + compartmentalization, can cause cytotoxicity and trigger either apoptotic or necrotic cell death.
Journal ArticleDOI
Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate.
TL;DR: It is reported here that micromolar concentrations of Ins1,4,5P3 release Ca2+ from a nonmitochondrial intracellular Ca2- store in pancreatic acinar cells, and the results strongly suggest that this is the same Ca1+ store that is released by acetylcholine.
Journal ArticleDOI
Store-operated calcium channels.
Anant B. Parekh,James W. Putney +1 more
TL;DR: The key electrophysiological features of I(CRAC) and other store-operated Ca(2+) currents and how they are regulated are described, and recent advances that have shed insight into the molecular mechanisms involved in this ubiquitous and vital Ca( 2+) entry pathway are considered.
Journal ArticleDOI
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
Christopher P. Baines,Robert A. Kaiser,Nicole H. Purcell,N. Scott Blair,Hanna Osinska,Michael Hambleton,Eric W. Brunskill,M. Richard Sayen,Roberta A. Gottlieb,Gerald W. Dorn,Jeffrey Robbins,Jeffery D. Molkentin +11 more
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
Related Papers (5)
A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporter
Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter
Joshua M. Baughman,Fabiana Perocchi,Fabiana Perocchi,Hany S. Girgis,Hany S. Girgis,Molly Plovanich,Molly Plovanich,Casey A. Belcher-Timme,Casey A. Belcher-Timme,Yasemin Sancak,Yasemin Sancak,X. Robert Bao,X. Robert Bao,Laura Strittmatter,Laura Strittmatter,Olga Goldberger,Olga Goldberger,Roman L. Bogorad,Victor Koteliansky,Vamsi K. Mootha,Vamsi K. Mootha +20 more